Frequency of monocyte subsets is linked to the severity of atherosclerosis in patients with ischemic heart disease: A case-control study.

BACKGROUND

Monocytes are recognized as central cells in the progression of atherosclerosis, and are subcategorized into classical (CD14++CD16), intermediate (CD14++CD16) and non-classical (CD14+CD16) subsets.

PURPOSE

The present study aimed to assess the relationships between different subsets of monocytes, metabolic and inflammatory factors in patients with stable coronary heart disease.

METHODS

A total of 26 patients (both men and women) with stable ischemic heart disease (IHD) were recruited. Among all the recruited patients, 17 patients had significant coronary artery disease defined as diameter stenosis more than 70%. Severity of CHD was assessed by the Gensini score (GS). Counts of CD14++CD16, CD14++CD16, and CD14+CD16 monocytes were evaluated by flow cytometry. Gating was verified and expression of CD163 was determined by imaging flow cytometry. Key cardiac markers, cytokines, and chemokines were detected in serum and in 24-hour-culture medium for peripheral blood mononuclear cells (PBMC) by multiplex analysis. The Mann-Whitney U-test and Spearman's rank correlation coefficient (r) were used for statistical analysis.

RESULTS

Patients with stenosis <70% tended to have higher frequency of CD14+CD16 monocytes compared to patients with coronary artery stenosis >70%. The frequencies of CD163+CD14++CD16 and CD163+CD14+CD16 monocytes were elevated in patients with stenosis >70%. In patients with stenosis <70%, the frequency of classical monocytes positively correlated and the frequency of non-classical monocytes negatively correlated with the value of GS (R =0.757; p =0.018 and R = -0.757; p = 0.018, respectively).

CONCLUSIONS

In patients with ischemic heart disease, the frequency of classical monocytes was directly correlated with the severity of atherosclerosis, while the frequency of non-classical monocytes was correlated inversely. The effects of these monocyte subsets in the development of myocardial ischemia still need to be elucidated.